Dementia:

It is a clinical syndrome, rather than a diagnosis in itself, which may cause by a variety of pathologies. Dementia is an acquire disorder, as distinct from learning disability in which impairments are present from birth, although the onset may be at any age. In a middle-aged or older person any social lapse that is out of character should always suggest dementia. [1]

Neoplastic dementias:

Types of Dementia:

1.Alzheimer’s Dementia:

This is the commonest cause of dementia, seen in about 70% of all cases of dementia in USA. It is more commonly seen in women. Earlier, it was differentiated into two forms: a presenile form and a senile

Neurochemically, there is a marked decrease in brain choline acetyltransferase (CAT) with a similar decrease in brain acetylcholinesterase (AchE).

Treatment:

Cholinesterase Inhibitors:

Rivastigmine(1.5 mg twice a day to 6 mg twice a day).

Donepezil(5-10 mg/day).

Galantamine (4 mg twice a day to 12 mg twice a day) have used in the recent past for treatment of moderate dementia with Alzheimer’s disease.

These elevate a cetylcholine (Ach) concentrations in cerebral cortex by slowing the degradation of acetylcholine released by still intact cholinergic neurons in Alzheimer’s disease.

Memantine (5-20 mg/day), an N-methyl-Daspartate (NMDA) antagonist, is also available for the treatment of moderately severe to severe Alzheimer’s disease.

2. Multi-infarct Dementia:

Multi-infarct dementia is the second commonest cause of dementia, seen in 10-15% of all cases, though it is probably more common in India. Occurrence of multiple cerebral infarctions can lead to a progressive disruption of brain function, leading to dementia.

The most typical form of multi-infarct dementia is characterise by the following features:

1. An abrupt onset.

2. Acute exacerbations (due to repeated infarct ions).

3. Stepwise clinical deterioration (step-ladder pattern).

4. Fluctuating course.

5. Presence of hypertension (most comm only) or any other signiﬁcant cardiovascular disease.

3. Hypothyroid Dementia:

This has been considered one of the most important treatable and reversible causes of dementia, second only to toxic dementias. Although it accounts for less than 1% of dementias, hypothyroidism should be suspected in every patient of dementia. Prompt treatment can reverse the dementing process and can lead to complete recovery if the treatment is start within two years of the onset of dementia.

4. AIDS Dementia Complex:

About 50-70% of patients suffering from AIDS exhibit a triad of cognitive, behavioural and motoric deﬁcits of subcortical dementia type and this is known as the AIDS-dementia complex (ADC).

As the AIDS virus (a lenti-virus, a type of retrovirus) is highly neurotropic and the virus crosses the blood-brain barrier early in the course of the disease cognitive impairment is nearly ubiquitous in AIDS.

Diagnosis: The diagnosis is establishe by ELISA (enzymelinked immuno-sorbent assay) showing anti-HIV antibodies, and the Western Blot test (blotting of antibody speciﬁcities to HIV-speciﬁc proteins). A Cranial CT scan can show cortical atrophy 1-4 months before the onset of clinical dementia while MRI scan is helpful in detecting the white matter lesions.

5. Lewy Body Dementia:

Lewy body dementia is now believe to be the second most common cause of the degenerative dementias, accounting for about 4% of all dementias.

Typically, the clinical features of Lewy body dementia include:

i. Fluctuating cognitive impairment over weeks or months, with involvement of memory and higher cortical functions (such as language, visuo-spatial ability, praxis and reasoning). Lucid intervals can be present in between ﬂ uctuations.

ii. Recurrent and detailed visual hallucinations.

iii. Spontaneous extrapyramidal or parkinsonian symptoms such as rigidity and tremors.

iv. Neuroleptic sensitivity syndrome, characterised by a marked sensitivity to the effects of typical doses of antipsychotic drugs (resulting in severe extrapyramidal side-effects with use of antipsychotics).

Although Lewy bodies (intra-cytoplasmic inclusion bodies) are also present in Parkinson’s disease, the occurrence of Lewy bodies in Lewy body dementia is more widespread. Antipsychotic medication should be avoided (or used with extreme caution and in low doses) in patients with Lewy body dementia.

Psychological:

Structured group cognitive stimulation programme

For agitation: aromatherapy, dance/music therapy, animal therapy

Psychological support for carers

Pharmacological:

Acetylcholinesterase inhibitors: (Donepezil, Galantamine, Rivastigmine) increase the concentration of and duration of action of acetylcholine in the central nervous system. There is evidence that in moderately severe Alzheimer’s disease, these drugs improve cognitive function and behaviour for up to a year. These drugs should only be prescribed by specialists, and should be stopped after 6 months if there is no clinical benefit.

Memantine: It is a glutamine NMDA receptor antagonist which improves cognition, mood, and behaviour in moderate to severe Alzheimer’s.

For agitation:

Antipsychotics : Antipsychotics should generally be avoided whenever possible and only have a role in patients with severely distressing symptoms or agitation causing risk to self or others. They should be avoided in those with mild to moderate dementia, as there is a slight increase in the risk of cerebrovascular events. The recommended drugs are haloperidol and olanzapine. A few patients need long-term oral antipsychotics to manage their behaviour at home.

Benzodiazepines: Benzodiazepines should be avoided wherever possible, especially during the day. Intramuscular lorazepam is a suitable alternative to an antipsychotic for extreme agitation, and should be tried if antipsychotics do not relieve the symptoms.